Neurofilament heavy phosphorylated epitopes as biomarkers in ageing and neurodegenerative disease.

From the day we are born, the nervous system is subject to insult, disease and degeneration. Aberrant phosphorylation states in neurofilaments, the major intermediate filaments of the neuronal cytoskeleton, accompany and mediate many pathological processes in degenerative disease. Neuronal damage, degeneration and death can release these internal components to the extracellular space and eventually the cerebrospinal fluid and blood.

Transition to shift work: Sleep patterns, activity levels, and physiological health of early-career paramedics.

The physiological impact of transitioning from full-time study to work in occupations that involve high-stress environments and shift work may plausibly impact sleep patterns and quality. There are limited studies focusing on the transition to shift work in graduate paramedics. This study aimed to assess early metabolic markers of health, activity, and sleep quality during the first 5 months of rostered shift work in a cohort of 28 graduate paramedics.

Coherence and cognition in the cortex: the fundamental role of parvalbumin, myelin, and the perineuronal net.

The calcium binding protein parvalbumin is expressed in interneurons of two main morphologies, the basket and chandelier cells, which target perisomatic domains on principal cells and are extensively interconnected in laminar networks by synapses and gap junctions. Beyond its utility as a convenient cellular marker, parvalbumin is an unambiguous identifier of the key role that these interneurons play in the fundamental functions of the cortex. They provide a temporal framework for principal cell activity by propagating gamma oscillation, providing coherence for cortical information processing and the basis for timing-dependent plasticity processes.

TDP-43 mislocalization drives neurofilament changes in a novel model of TDP-43 proteinopathy.

Mislocalization of the TAR DNA-binding protein 43 (TDP-43) from the nucleus to the cytoplasm is a common feature of neurodegenerative conditions such as amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). The downstream cellular effects of this mislocalization are not well understood. To investigate the impact of mislocalized TDP-43 on neuronal cell bodies, axons and axonal terminals, we utilized the mouse visual system to create a new model of TDP-43 proteinopathy.

Age Moderates the Effects of Traumatic Brain Injury on Beta-Amyloid Plaque Load in APP/PS1 Mice.

Traumatic brain injury (TBI) has been identified as a risk factor for Alzheimer's disease (AD). However, how such neural damage contributes to AD pathology remains unclear; specifically, the relationship between the timing of a TBI relative to aging and the onset of AD pathology is not known. In this study, we have examined the effect of TBI on subsequent beta-amyloid (Aβ) deposition in APP/PS1 (APP/PSEN1dE9) transgenic mice either before (3 months of age) or after the onset (6 months of age) of plaque pathology.